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Background Health disparities among minority groups, especially African Americans, can limit their access to quality medical care and lead to disproportionate medical management and disease outcomes. The aim of this study was to compare the COVID-19-related change in mammogram volumes and cancer detection at two affiliated academic breast centers, one that serves a predominantly African American patient population and one that serves a predominantly non-African American patient population. Materials and methods For the purpose of anonymity, racial demographics were collected and the center with a higher African American patient population was designated as institution A, while the center with a higher non-African American patient population was designated as institution B. Careful selection of the two breast centers was instituted in order to limit the impact of potential confounders other than race. An Institutional Review Board (IRB) exemption was obtained and two Mammography Quality Standards Act (MQSA) reports were generated; one for March 2020 through September 2020, during the height of the COVID-19 pandemic, and one for March 2019 through September 2019 to serve as the pre-pandemic control group. The i2b2 Query Analysis Tool® was used to obtain racial demographic data and compare the percent change in screening and diagnostic mammograms, image-guided biopsies, total cancers diagnosed by imaging, and percent of minimal cancers for both institutions. Results Screening mammograms and breast cancer detection decreased in 2020 compared to 2019 at both institutions. However, the percent change from 2019 to 2020 was greater at institution A than at institution B. Percent minimal cancers, an indicator of early-stage breast cancer also decreased more drastically at institution A than at institution B. Interestingly, the total number of diagnostic exams and image-guided biopsies increased in 2020 at institution B, whereas both decreased at institution A. Conclusion The COVID-19 pandemic may lead to worsening racial disparities in breast cancer screening. In an effort to narrow future disparity, it is crucial for radiologists and other health care providers to be aware of this inequality and educate all women on the importance of obtaining routine screening mammography. More studies are needed.

ObjectivePatients with myelin oligodendrocyte glycoprotein antibody (MOG‐IgG)‐associated disease (MOGAD) suffer from severe optic neuritis (ON) leading to retinal neuro‐axonal loss, which can be quantified by optical coherence tomography (OCT). We assessed whether ON‐independent retinal atrophy can be detected in MOGAD.MethodsEighty patients with MOGAD and 139 healthy controls (HCs) were included. OCT data was acquired with (1) Spectralis spectral domain OCT (MOGAD: N = 66 and HCs: N = 103) and (2) Cirrus high‐definition OCT (MOGAD: N = 14 and HCs: N = 36). Macular combined ganglion cell and inner plexiform layer (GCIPL) and peripapillary retinal nerve fiber layer (pRNFL) were quantified.ResultsAt baseline, GCIPL and pRNFL were lower in MOGAD eyes with a history of ON (MOGAD‐ON) compared with MOGAD eyes without a history of ON (MOGAD‐NON) and HCs (p < 0.001). MOGAD‐NON eyes had lower GCIPL volume compared to HCs (p < 0.001) in the Spectralis, but not in the Cirrus cohort. Longitudinally (follow‐up up to 3 years), MOGAD‐ON with ON within the last 6–12 months before baseline exhibited greater pRNFL thinning than MOGAD‐ON with an ON greater than 12 months ago (p < 0.001). The overall MOGAD cohort did not exhibit faster GCIPL thinning compared with the HC cohort.InterpretationOur study suggests the absence of attack‐independent retinal damage in patients with MOGAD. Yet, ongoing neuroaxonal damage or edema resolution seems to occur for up to 12 months after ON, which is longer than what has been reported with other ON forms. These findings support that the pathomechanisms underlying optic nerve involvement and the evolution of OCT retinal changes after ON is distinct in patients with MOGAD. ANN NEUROL 2022;92:476–485

Abstract Background: Genome-wide association studies (GWAS) of multiple myeloma in populations of European ancestry (EA) identified and confirmed 24 susceptibility loci. For other cancers (e.g., colorectum and melanoma), risk loci have also been associated with patient survival. Methods: We explored the possible association of all the known risk variants and their polygenic risk score (PRS) with multiple myeloma overall survival (OS) in multiple populations of EA [the International Multiple Myeloma rESEarch (IMMEnSE) consortium, the International Lymphoma Epidemiology consortium, CoMMpass, and the German GWAS] for a total of 3,748 multiple myeloma cases. Cox proportional hazards regression was used to assess the association between each risk SNP with OS under the allelic and codominant models of inheritance. All analyses were adjusted for age, sex, country of origin (for IMMEnSE) or principal components (for the others) and disease stage (ISS). SNP associations were meta-analyzed. Results: SNP associations were meta-analyzed. From the meta-analysis, two multiple myeloma risk SNPs were associated with OS (P &lt; 0.05), specifically POT1-AS1-rs2170352 [HR = 1.37; 95% confidence interval (CI) = 1.09–1.73; P = 0.007] and TNFRSF13B-rs4273077 (HR = 1.19; 95% CI = 1.01–1.41; P = 0.04). The association between the combined 24 SNP MM-PRS and OS, however, was not significant. Conclusions: Overall, our results did not support an association between the majority of multiple myeloma risk SNPs and OS. Impact: This is the first study to investigate the association between multiple myeloma PRS and OS in multiple myeloma.

7514 Background: The AETHERA trial demonstrated improvement in PFS with 16 cycles of brentuximab vedotin (BV) after autologous stem cell transplant (ASCT) in BV-naive patients with high-risk relapsed/refractory classical Hodgkin lymphoma (r/r cHL). However, in real world, patients are rarely able to complete all 16 cycles of BV at full dose. We performed a multicenter retrospective study to assess the impact of cumulative dose on toxicity and 2-year PFS. Methods: Patients from 11 institutions across the US who had received at least one cycle of BV maintenance after ASCT for r/r cHL with one of these features were included: primary refractory disease (PRD), extra-nodal disease (END), or relapse < 12 months of diagnosis (RL<12). PFS was compared between the three cohorts based on a total cumulative dose of 28.8 mg/kg (1.8 mg/kg x 16 cycles): C1, those that received >75% (21.7 to 28.8 mg/kg) cumulative dose of BV, C2, those that received between 51% -75% (14.5 to 21.6 mg/kg) dose and C3, those that received ≤ 50% (≤ 14.4 mg/kg) dose. Results: Between July 2015-June 2019, 100 patients with a median age of 34 years (19-70) underwent ASCT for r/r cHL. At relapse, 44% had PRD, 47% had RL<12, 39% had END and 45% had received BV as initial (1%) or salvage (44%) therapy. 71% had CR before ASCT and 23% received >1 line of salvage (>1 SLT). There was no difference in baseline characteristics between the cohorts. Thirty-six patients were in C1, 27 in C2, and 37 in C3. Only 14% of patients received full cumulative dose of BV. The median number of cycles completed was 12. Fifty-seven patients discontinued early: 39 for toxicity, 7 for progression, 5 for patient preference, 2 for cost and 4 for other reasons. Six of the patients who stopped early for progression were in C3. Grade ≥3 adverse events for neuropathy, neutropenia, and infections were 16%, 7%, and 5% respectively. There was no difference in severity of neuropathy in patients who had received BV prior to ASCT (p=.37). The median follow up was 3.37 years (.4–6.35). The 2-year PFS was 85% for all subjects, 94% for C1, 84% for C2, and 72% for C3 (p=.079) (Table). Patients in C3 had worse PFS compared to C1 (p=.035); this difference remained significant after adjusting for five other factors. There was no difference in PFS between C1 and C2 (p=.29). Conclusions: The majority of patients discontinued BV maintenance early due to toxicity. 2-year PFS was robust regardless of cumulative dose of BV. We conclude that total cumulative dose of 28.8 mg/kg of BV maintenance is not necessary and 51%-75% of total BV dose may still attain a similar PFS advantage. [Table: see text]

e16168 Background: Several fibroblast growth factor receptor (FGFR) inhibitors have been recently approved or are in development for the treatment of cholangiocarcinoma (CCA) with FGFR2 fusions/rearrangements (f/r), such as the ATP-competitive inhibitors pemigatinib and infigratinib (FDA-approved in 2020/2021) and the covalent inhibitor futibatinib, which has shown efficacy in a pivotal phase 2 trial. To inform future evaluations of the impact of these agents in clinical practice, and understand other existing gaps in care, we investigated the characteristics and clinical management of patients with CCA and FGFR2 f/r prior to 2021. Methods: This real-world, retrospective cohort study used de-identified, patient-level electronic health records data from Cancer Treatment Centers of America (CTCA) to identify adults with a diagnosis of advanced intrahepatic CCA (iCCA) who received genomic testing between 2013-2021. Clinical/demographic characteristics, time to genomic testing, treatment patterns, and outcomes of patients with and without FGFR2 f/r were described. Results: 23 patients with FGFR2 f/r and 88 with FGFR wild-type (wt) iCCA were identified. Compared to FGFR wt, FGFR2 f/r had a higher proportion of female (65.2 vs 45.5%) and Black (39.1 vs 18.2%) patients (Table). Mean age at diagnosis was ̃60 y and >60% were diagnosed with stage 4 disease in both cohorts; 91.3% of f/r and 78.4% of wt patients had an ECOG PS 0/1. Median time from diagnosis to genomic testing was ̃5 mo; upon entry to CTCA, median time to testing was <2 mo. 17/23 patients in the f/r cohort had FGFR2 fusions (4 BICC1, 13 other). Three FGFR2 f/r patients received an FGFR inhibitor (pemigatinib) as next treatment after testing in 2020. A trend towards longer median overall survival in the f/r vs wt group (24.5 vs 17.8 mo), and a correlation of survival with ECOG PS were observed. Conclusions: This analysis provides insight into the real-world characteristics, clinical management and outcomes among patients with iCCA and FGFR2 f/r, predominantly prior to the introduction of FGFR inhibitors, providing a baseline for further study as the treatment landscape evolves. Of note, the time lag between diagnosis and genomic testing before entry to CTCA underlines the need for earlier testing to guide optimal therapy in clinical practice. [Table: see text]

Key Points Identifying ways to prevent AKI may reduce mortality further in the setting of intensive BP control. Creatinine-based ascertainment of AKI, enabled by electronic health record data, may be more sensitive and less biased than traditional serious adverse event adjudication. Background Adjudication of inpatient AKI in the Systolic Blood Pressure Intervention Trial (SPRINT) was based on billing codes and admission and discharge notes. The purpose of this study was to evaluate the effect of intensive versus standard BP control on creatinine-based inpatient and outpatient AKI, and whether AKI was associated with cardiovascular disease (CVD) and mortality. Methods We linked electronic health record (EHR) data from 47 clinic sites with trial data to enable creatinine-based adjudication of AKI. Cox regression was used to evaluate the effect of intensive BP control on the incidence of AKI, and the relationship between incident AKI and CVD and all-cause mortality. Results A total of 3644 participants had linked EHR data. A greater number of inpatient AKI events were identified using EHR data (187 on intensive versus 155 on standard treatment) as compared with serious adverse event (SAE) adjudication in the trial (95 on intensive versus 61 on standard treatment). Intensive treatment increased risk for SPRINT-adjudicated inpatient AKI (HR, 1.51; 95% CI, 1.09 to 2.08) and for creatinine-based outpatient AKI (HR, 1.40; 95% CI, 1.15 to 1.70), but not for creatinine-based inpatient AKI (HR, 1.20; 95% CI, 0.97 to 1.48). Irrespective of the definition (SAE or creatinine based), AKI was associated with increased risk for all-cause mortality, but only creatinine-based inpatient AKI was associated with increased risk for CVD. Conclusions Creatinine-based ascertainment of AKI, enabled by EHR data, may be more sensitive and less biased than traditional SAE adjudication. Identifying ways to prevent AKI may reduce mortality further in the setting of intensive BP control.

Abstract There is great interest in expanding the use of ultrasound (US), but new challenges exist with its application to lumbar facet–targeted procedures. The primary aim of this systematic review and meta-analysis was to determine the risk of incorrect needle placement associated with US–guided lumbar medial branch blocks (MBB) and facet joint injections (FJI) as confirmed by fluoroscopy or computerized tomography (CT). An a priori protocol was registered, and a database search was conducted. Inclusion criteria included all study types. Risk of bias was assessed using the Cochrane risk of bias tool for randomized controlled trials and the National Heart, Lung, and Blood tool for assessing risk bias for observational cohort studies. Pooled analysis of the risk difference (RD) of incorrect needle placement was calculated. Pooled analysis of 7 studies demonstrated an 11% RD (P < 0.0009) of incorrect needle placement for US-guided MBB confirmed using fluoroscopy with and without contrast. Pooled analysis of 3 studies demonstrated a 13% RD (P < 0.0001) of incorrect needle placement for US-guided FJI confirmed using CT. The time to complete a single-level MBB ranged from 2.6 to 5.0 minutes. The certainty of evidence was low to very low. Ultrasound-guided lumbar MBB and FJI are associated with a significant risk of incorrect needle placement when confirmed by fluoroscopy or CT. The technical limitations of US and individual patient factors could contribute to the risk of incorrect needle placement.